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Investigating potential mechanisms of vitamin D against thyroid cancer via network pharmacology and experimental
Abstract:
Thyroid cancer (TC) is one of the most common endocrine malignancies worldwide. Increasing evidence suggests that vitamin D (VD) has potential benefits in the treatment of TC. However, evidence regarding the targets and molecular mechanisms of VD in TC remains limited. In this study, we conducted network pharmacology, molecular docking, and experimental evaluation to explore the target genes, biological functions, and signaling pathways involved in this process. Network analysis revealed 77 potential target genes of VD against TC, and four hub target genes were identified: ESR1, KIT, CCND1, and PGR. Furthermore, we identified the biological processes (BP) and signaling pathways involving these potential target genes, and then determined the possible interaction between the hub targets and VD through molecular docking. Finally, through in vitro experiments, we found that VD effectively inhibits the proliferation of TC cells and downregulates the expression of the ESR1 gene. In conclusion, the effects of VD against TC involve multiple biological targets, BP, and signaling pathways. These findings provide scientific evidence for the application of VD in the treatment of TC.
Insights
Vitamin D (VD) shows promise for treating thyroid cancer (TC). This study identified key molecular targets and confirmed VD inhibits TC cell proliferation, offering new therapeutic insights.
Area of Science:
- Endocrinology
- Molecular Biology
- Pharmacology
Background:
- Thyroid cancer (TC) is a prevalent endocrine malignancy globally.
- Vitamin D (VD) is increasingly recognized for its potential therapeutic benefits in TC.
- Limited understanding exists regarding VD's specific molecular targets and mechanisms in TC.
Purpose of the Study:
- To elucidate the molecular targets, biological functions, and signaling pathways of VD in TC.
- To investigate the interaction between VD and its potential targets using computational and experimental methods.
- To provide a scientific basis for VD's application in TC treatment.
Main Methods:
- Network pharmacology was employed to identify potential target genes of VD against TC.
- Molecular docking was used to assess the interaction between VD and identified hub target genes.
- In vitro experiments were conducted to validate the effects of VD on TC cell proliferation and gene expression.
Main Results:
- Network analysis identified 77 potential target genes, with ESR1, KIT, CCND1, and PGR highlighted as key hub targets.
- Molecular docking suggested possible interactions between VD and these hub targets.
- In vitro studies demonstrated that VD significantly inhibits TC cell proliferation and reduces ESR1 gene expression.
Conclusions:
- Vitamin D exerts its anti-thyroid cancer effects through multiple biological targets, processes, and pathways.
- The study identified specific molecular mechanisms, including the downregulation of ESR1, by which VD impacts TC.
- These findings support the potential of VD as a therapeutic agent for thyroid cancer.
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